Аннотация:Activation of neutrophils is accompanied by the oxidative burst, exocytosis of various granule types (degranulation) and a delay in spontaneous apoptosis. The major source of reactive oxygen species (ROS) in human neutrophils is NADPH oxidase (NOX2), however, other sources of ROS also exist. Although the function of ROS is mainly defensive, they can also play a regulatory role in cell signaling. However, the contribution of various sources of ROS in these processes is not clear. A possible role of mitochondria-derived ROS (mtROS) in the regulation of neutrophil activation induced by chemoattractant fMLP in vitro was investigated. Using the mitochondria-targeted antioxidant SkQ1 (plastoquinone conjugated with decyltriphenylphosphonium), which was developed at Moscow University, the implication of mtROS in the oxidative burst caused by NOX2 activation as well as in the exocytosis of primary (azurophil) and secondary (specific) granules, was demonstrated. Scavenging of mtROS with SkQ1 slightly accelerated spontaneous apoptosis and significantly stimulated apoptosis of fMLP-activated neutrophils. According to the data obtained, mtROS play a critical role in signal transduction that mediates the major neutrophil functional responses in the process of activation. Scavenging of mtROS with the mitochondria-targeted antioxidants may be envisaged as a novel strategy for treating a variety of diseases associated with excessive activation of neutrophils.